Severe tuberculosis induces unbalanced up-regulation of gene networks and overexpression of IL-22, MIP-1alpha, CCL27, IP-10, CCR4, CCR5, CXCR3, PD1, PDL2, IL-3, IFN-beta, TIM1, and TLR2 but low antigen-specific cellular responses.

@article{Qiu2008SevereTI,
  title={Severe tuberculosis induces unbalanced up-regulation of gene networks and overexpression of IL-22, MIP-1alpha, CCL27, IP-10, CCR4, CCR5, CXCR3, PD1, PDL2, IL-3, IFN-beta, TIM1, and TLR2 but low antigen-specific cellular responses.},
  author={Liyou Qiu and Dan ” Huang and Cystal Y Chen and Richard C. Wang and Ling Shen and Yun Hui Shen and Robert C. Hunt and James Estep and Barton F. Haynes and William Robert Jacobs and Norman L. Letvin and George Du and Z Chen},
  journal={The Journal of infectious diseases},
  year={2008},
  volume={198 10},
  pages={1514-9}
}
The immune mechanisms by which early host-mycobacterium interaction leads to the development of severe tuberculosis (TB) remain poorly characterized in humans. Here, we demonstrate that severe TB in juvenile rhesus monkeys down-regulated many genes in the blood but up-regulated selected genes constituting gene networks of Th17 and Th1 responses, T cell activation and migration, and inflammation and chemoattractants in the pulmonary and lymphoid compartments. Overexpression (450-2740-fold) of 13… CONTINUE READING

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